Mydriasis/mɨˈdraɪ.əsɪs/ is the dilation of the pupil, usually defined as when having a non-physiological cause,[1] but sometimes defined as potentially being a physiological pupillary response.[2] Non-physiological causes of mydriasis include disease, trauma, or the use of drugs. Normally, as part of the pupillary light reflex, the pupil dilates in the dark and constricts in the light to respectively improve vividity at night and to protect the retina from sunlight damage during the day. A mydriatic pupil will remain excessively large even in a bright environment. The excitation of the radial fibres of the iris which increases the pupillary aperture is referred to as a mydriasis. More generally, mydriasis also refers to the natural dilation of pupils, for instance in low light conditions or under sympathetic stimulation.

An informal term for mydriasis is blown pupil,[3] and is used by medical providers. It is usually used to refer to a fixed, unilateral mydriasis, which could be a symptom of raised intracranial pressure.

The opposite, constriction of the pupil, is referred to as miosis. Both mydriasis and miosis can be physiological. Anisocoria is the condition of one pupil being more dilated than the other.

The mechanism of mydriasis depends on the agent being used. It usually involves either a disruption of the parasympathetic nerve supply to the eye (which normally constricts the pupil) or overactivity of the sympathetic nervous system (SNS).

Natural release of the hormone oxytocin can cause mild to moderate mydriasis. Strong sexual arousal can often lead to very enlarged pupils, rather than the minor dilation observed during sexual affection. [n 1]

The parasympathetic nervous supply, which causes constriction of the pupil, or miosis, is supplied by cranial nerve III, the oculomotor nerve. Damage to this nerve typically manifests itself as mydriasis, because the sympathetic supply to the pupil, which causes mydriasis, remains unaffected, and therefore unopposed.

The neurotransmitternorepinephrine regulates many physiological processes in the body and brain. One of them is the autonomic constriction and contraction of certain muscles. The psychoactive drug cocaine potently inhibits the normal reuptake of norepinephrine into presynaptic nerve terminals, resulting in an increased level of extracellular norepinephrine. Amphetamines also potently release and prevent the reuptake of norepinephrine. The released norepinephrine then proceeds to bind to adrenergic receptors, and the biological effects of norepinephrine finally occur. When a solution of cocaine is dropped into the eye, this process takes place and the end result is dilation of the pupil. Cocaine itself is not typically used for this task, however. Any potent norepinephrine reuptake inhibitor or release agent should be capable of such an effect.

^Orgasm has been reported to lead to pupillary block[4] in a single case in combination with an ocular precondition. Here the parasympathetic and sympathetic stimulation lead to sphincter muscle stimulation during pupillary dilation in the dark, while ciliary contraction caused zonular relaxation leading to pupillary block and angle-closure in combination with pre-existing narrow chamber angle.